氟化钠致大鼠肾脏脂质过氧化损伤及亚硒酸钠的保护作用

目的研究氟化钠（ＮａＦ）对大鼠肾脏脂质过氧化作用的影响及亚硒酸钠（Ｎａ２ＳｅＯ３）对氟肾脏毒性的保护作用。方法大鼠经饮水加入ＮａＦ（１５ｍｍｏｌ／Ｌ）或／和Ｎａ２ＳｅＯ３（１５μｍｏｌ／Ｌ）染毒１２０天,观察氟在机体的蓄积、排泄,尿酶活性及肾脏脂质过氧化水平的变化。结果氟染毒后,大鼠血氟水平、尿氟水平、骨氟含量,尿谷氨酰转肽酶（γＧＴ）、Ｎ乙酰βＤ氨基葡萄糖苷酶（ＮＡＧ）、琥珀酸脱氢酶（ＳＤＨ）活性及肾脏活性氧自由基（ＯＦＲＳ）相对浓度、脂质过氧化降解产物丙二醛（ＭＤＡ）含量均显著升高,谷胱甘肽过氧化物酶（ＧＳＨＰｘ）活性及ＧＳＨ含量显著下降。同时补加亚硒酸钠,可促进尿氟排泄,降低血氟水平及骨氟含量,降低尿酶γＧＴ、ＮＡＧ、ＳＤＨ活性和肾脏ＯＦＲＳ、ＭＤＡ含量,同时提高肾脏ＧＳＨＰｘ活性,但对ＧＳＨ含量影响不显著。结论氟化钠引起肾脏损伤与其诱导脂质过氧化作用增强有关,亚硒酸钠对氟化钠致肾脏毒性具有拮抗作用。     

缺锌对大鼠脂质过氧化及抗氧化系统的影响

研究缺锌对３周龄大鼠的脂质过氧化和抗氧化系统的影响。方法：健康Ｗｉｓｔａｒ大鼠３３只,雌雄各半,按体重随机分为Ａ（缺锌组）,Ｂ（自由进食对照组）,Ｃ（配对喂养组）。每组１１只,实验期４０天。观察指标有血清和肝脏锌,肝脏超氧化物歧化酶（ＳＯＤ）、谷胱甘肽过氧化物酶（ＧＳＨ－Ｐｘ）活性,血清和肝脏丙二醛（ＭＤＡ）,并采用电子自旋共振（ｅｌｅｃｔｒｏｎｓｐｉｎｒｅｓｏｎａｎｃｅ,ＥＳＲ）及自旋捕捉技术直接测定大鼠肝组织中的氧自由基。结果：Ａ组大鼠肝脏ＳＯＤ、ＧＳＨ－Ｐｘ活性明显下降,血清和肝脏ＭＤＡ含量显著升高,ＥＳＲ图谱出现了Ｎ－Ｈ偶合的三组双峰波。结论：缺锌可以使大鼠脂质过氧化反应明显加强,而抗氧化能力明显减弱。     

β-胡萝卜素对二甲基亚硝胺致大鼠脂质过氧化的影响

探讨了给予二甲基亚硝胺（ＮＤＭＮ），同时补充β－胡萝卜素（β－Ｃ）后，大鼠体内抗氧化酶活性和脂质过氧化物含量的变化。结果显示，一定剂量的ＮＤＭＮ可使大鼠血红细胞、肝肾匀浆ＳＯＤ活性和全血ＧＳＨ－Ｐｘ活性下降（Ｐ＜０．０５），血清和肝ＭＤＡ和血清ＲＯＯＨ产生增多（Ｐ＜０．０５）。添加β－Ｃ（２５ｍｇ／ｋｇ）后，ＳＯＤ和ＧＳＨ－Ｐｘ活性均比单纯ＮＤＭＮ组有明显提高（Ｐ＜０．０５）。ＭＤＡ和ＲＯＯＨ含量明显低于ＮＤＭＮ组（Ｐ＜０．０５）。提示自由基和脂质过氧化反应可能也是ＮＤＭＮ及其它亚硝胺致癌的途径之一；一定剂量的β－Ｃ可对抗ＮＤＭＮ引起的自由基和脂质过氧化。     

β-胡萝卜素和核黄素对大鼠脂质过氧化的影响

目的：进一步探讨亚硝胺通过脂质过氧化而致癌的可能途径,以及研究β－胡萝卜素（β－Ｃ）和核黄素（ＶＢ２）通过抑制脂质过氧化反应而影响亚硝胺致癌的可能途径。方法：将５０只二级ＳＤ雄性大鼠随机分成５组。实验组在每日灌胃二甲基亚硝胺（ＮＤＭＮ）１．７５ｍｇ／ｋｇ的基础上,每日分别给予β－Ｃ２５ｍｇ／ｋｇ和／或ＶＢ２１８ｍｇ／ｋｇ补充,实验期为２８天。实验结束时,收集血液,摘取肝脏和肾脏,测红细胞和肝肾匀浆ＳＯＤ活性,全血ＧＳＨ－Ｐｘ活性,血清和肝肾匀浆ＭＤＡ含量,血清ＲＯＯＨ以及全血Ｈｂ含量。结果：１．ＮＤＭＮ可使ＳＯＤ和ＧＳＨ－Ｐｘ活性下降（Ｐ＜０．０５）,ＭＤＡ和ＲＯＯＨ产生增多（Ｐ＜０．０５）。２．添加β－Ｃ后,ＳＯＤ和ＧＳＨ－Ｐｘ活性有明显提高（Ｐ＜０．０５）,ＭＤＡ和ＲＯＯＨ的含量明显降低（Ｐ＜０．０５）。３．添加ＶＢ２后,肝ＳＯＤ和全血ＧＳＨ－Ｐｘ活性均有明显提高（Ｐ＜０．０５）,但ＭＤＡ和ＲＯＯＨ的含量没有差异（Ｐ＞０．０５）。４．同时补充β－Ｃ和ＶＢ２后,各项指标的变化与单纯β－Ｃ组基本一致。结论：脂质过氧化也是亚硝胺致癌的途径之一;一定剂量的β－Ｃ可对抗ＮＤＭＮ引发的脂质过氧化;核黄素对提高抗氧化?     

硒、维生素E对心肌胶原蛋白代谢的影响

目的：阐明硒（Ｓｅ）、维生素Ｅ（ＶＥ）与心肌胶原蛋白代谢的关系。方法：以病区粮（低Ｓｅ、低ＶＥ）喂养大鼠,并注射异丙基肾上腺素（ＩＳＯ）诱发心肌缺血缺氧性坏死,检测心肌中谷胱甘肽氧化酶（ＧＳＨ－ＰＸ）、过氧化氢酶（ＣＡＴ）、丙二醛（ＭＤＡ）和胶原蛋白含量变化。结果：低Ｓｅ低ＶＥ组血浆和心肌ＧＳＨ－ＰＸ、ＣＡＴ活性下降,ＭＤＡ含量上升,与心肌胶原蛋白含量变化有相关性。补Ｓｅ补ＶＥ后,ＧＳＨ－ＰＸ、ＣＡＴ活性上升,ＭＤＡ水平下降,心肌胶原蛋白含量下降。结论：低Ｓｅ低ＶＥ加重ＩＳＯ诱发的心肌损伤,脂质过氧化和自由基与心肌胶原蛋白代谢关系密切。补Ｓｅ补ＶＥ后,能缓解心肌细胞对诱发因素所造成的损伤,对保护心肌细胞和防止心肌纤维化的形成具有一定作用。     

硒强化沙棘果汁对大鼠机体脂质过氧化作用的影响

成年Ｗｉｓｔａｒ大鼠用含硒强化沙棘果汁、沙棘果汁及维生素Ｃ的半纯化饲料喂养１２周后，测定其血清、肝脏和红细胞膜丙二醛（ＭＤＡ）含量，全血及肝脏谷胱甘肽过氧化物酶（ＧＳＨ－Ｐｘ）活性及全血超氧化物岐化酶（ＳＯＤ）活性的变化。结果表明：大鼠血清、肝脏及红细胞膜ＭＤＡ含量在各实验组均远远低于对照组（Ｐ＜０．０１）。而各实验组ＧＳＨ－Ｐｘ和ＳＯＤ活性均显著高于对照组。结果说明，沙棘果汁可显著降低大鼠机体内脂质过氧化反应，增强机体抵抗过氧化损伤的能力，这种作用在经硒强化后尤为显著。     

矽肺与NO、氧化及脂质过氧化关系的探讨

目的探讨矽肺与ＮＯ及氧化和脂质过氧化的关系。方法检测７３例矽肺患者和６０例健康对照者的血浆ＮＯ、ＶｉｔＣ、ＶｉｔＥ、β胡萝卜素（βＣＡＲ）、过氧化脂质（ＬＰＯ）含量及红细胞超氧化物歧化酶（ＳＯＤ）、过氧化氢酶（ＣＡＴ）、谷胱甘肽过氧化物酶（ＧＳＨＰｘ）活力和ＬＰＯ含量。结果与对照组比较,矽肺组的血浆ＶｉｔＣ、ＶｉｔＥ、βＣＡＲ含量及红细胞ＳＯＤ、ＣＡＴ、ＧＳＨＰｘ活力显著降低,血浆ＮＯ、ＬＰＯ含量及红细胞ＬＰＯ含量显著升高（Ｐ＜０．０５或Ｐ＜０．０１）;各检测值与病程均有相关;血浆ＮＯ、ＶｉｔＥ含量及红细胞ＳＯＤ活力、ＬＰＯ含量与病程相关最密切。结论矽肺患者体内的ＮＯ代谢异常,氧化和脂质过氧化反应病理性加剧。     

苦荞蛋白复合物的营养成分及其抗衰老作用的研究

分析苦荞蛋白复合物的营养成分,观察其抗衰老效果。方法：用碱抽提和等电点沉淀法从苦荞麦籽粒中制备出苦荞蛋白复合物（ＴＢＰＣ）,再用含２０％ＴＢＰＣ饲料喂小鼠,观察对小鼠血液和脏器中超氧化物岐化酶（ＳＯＤ）、过氧化氢酶（ＣＡＴ）和谷胱苷肽过氧化物酶（ＧＳＨ－Ｐｘ）的活性的影响。结果：ＴＢＰＣ的蛋白质含量为６３．４％,脂肪１２．７％,碳水化物１０．２％,灰分３．５％,粗纤维０．４％,水分９．８％。用ＴＢＰＣ饲喂后,小鼠血液、肝脏和心脏中ＳＯＤ、ＣＡＴ和ＧＳＨ－Ｐｘ活性均有不同程度提高,脂质过氧化产物丙二醛（ＭＤＡ）含量下降。结论：苦荞蛋白复合物对生物体有一定营养和抗衰老作用。     

绿茶及混合茶抑制二乙基亚硝胺诱发大鼠肝癌前期病变的抗氧化机理研究

用二乙基亚硝胺（ＤＥＮ）诱发Ｗｉｓｔａｒ大鼠肝癌前期病变（Ｓｏｌｔ－Ｆａｒｂｅｒ模型）。实验前６周给大鼠饮用２％绿茶水及０．５％混合茶水，于实验第８周末宰杀动物。结果发现，绿茶组及混合茶组肝ｒ－ＧＴ异常病灶数均明显低于阳性对照组（Ｐ＜０．０１）。经ＨＰＬＣ法分离肝微粒体脂质过氧化产物丙二醛（ＭＤＡ）、乙醛（ＡＣＴ）、戊醛（ＰＰ）、丙酮（ＡＣＯＮ），与阳性对照组相比，绿茶组和混合茶组的各种脂质过氧化产物均有不同程度的降低。此外，对多种抗氧化酶和Ⅱ相代谢酶活性进行检测，其中绿茶组ＳＯＤ、ＧＳＴ、ＱＲ活性明显高于阳性对照组；混合茶组ＣＡＴ、ＳＯＤ、ＧＳＴ、ＱＲ活性明显高于阳性对照组。结果表明，绿茶和混合茶对ＤＥＮ诱发大鼠肝癌的发生均有显著的预防作用。其作用机理可能和诱导抗氧化酶及某些Ⅱ相代谢酶活性，以及抑制脂质过氧化作用有关。     

微量元素硒对动脉粥样硬化家兔内皮素的影响

用放免分析方法，对服Ｓｅ的动脉粥样硬化（ＡＳ）家兔血浆内皮素（ＥＴ）水平进行测定。结果表明，Ｓｅ组家兔血浆ＥＴ水平明显低于对照组，同时血清胆固醇（Ｃｈ）、低密度脂蛋白（ＬＤＬ）及过氧化脂质（ＬＰＯ）含量降低，高密度脂蛋白（ＨＤＬ）明显增高，全血谷胱甘肽过氧化物酶（ＧＳＨ－Ｐｘ）和血清超氧化物歧化酶（ＳＯＤ）活力也明显提高。提示，Ｓｅ可通过抗氧化作用保护内皮细胞免遭过氧化损伤，减少ＥＴ释放，抑制ＡＳ形成和发展。     

硒对镉在大鼠肝脏亚细胞分布及脂质过氧化作用的影响

采用给大鼠腹腔注射镉(CdCl_2 1mg/kg)或/和硒(Na_2SeO_3 0.4mg/kg)的方法,研究了硒对镉在大鼠肝脏亚细胞分布及脂质过氧化作用的影响。结果表明,给大鼠连续腹腔注射CdCl_2(1mg/kg)3d,可致大鼠肝微粒体和线粒体脂质过氧化物(LPO)含量显著增加,谷胱甘肽过氧化物酶(GSH-Px)活性显著下降,肝细胞浆还原型谷胱甘肽(GSH)含量显著降低。同时给大鼠腹腔注射Na_2SeO_3(0.4mg/kg),硒可拮抗上述镉的效应。但硒对大鼠肝脏镉含量及镉在肝脏亚细胞分布没有明显影响。     

Oxidative stress and endocrine endpoints in white sucker (Catostomus commersoni) from a river impacted by agricultural chemicals

The effects of agricultural chemicals on cortisol secretion, antioxidants, and lipid peroxidation were investigated in hepatic and adrenal tissue of white sucker (Catostomus commersoni) from a river (Yamaska) that drains an agricultural region in Québec (Canada). Plasma cholinesterase (ChE) activity, used as a biomarker of exposure to pesticides, was elevated in fish from the reference site compared to fish from the contaminated sites. Plasma concentrations of cortisol and thyroid hormones (T3 and T4) were higher in fish from the reference site compared to contaminated sites; reduced glutathione (GSH) levels, catalase (CAT), and glutathione peroxidase (GPx) activities were higher and lipid peroxidation (LPO) was lower. Levels of antioxidants (CAT, Gpx, and GSH) were higher (10-90%) and LPO levels were lower (50%) in the liver than in the adrenal tissue. The present in situ study provided evidence that antioxidants, lipid peroxidation, and plasma hormones were altered in fish sampled in areas impacted by agricultural chemicals. Endocrine-disrupting effects were associated with oxidative stress. The results suggest that antioxidants and lipid peroxidation could be used as markers of contaminant exposure in fish.     

Effects of vitamins E and A on 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD)-induced lipid peroxidation and other biochemical changes in the rat

The effects of vitamins A and E on 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD)-induced lipid peroxidation in the rat were investigated. Vitamin E markedly inhibited microsomal lipid peroxidation (malondialdehyde formation), but had no effect on glutathione peroxidase activity or glutathione (GSH) content, and did not protect against decreased body and liver weights. Furthermore, vitamin E had little effect on TCDD-induced lethality in rats. Vitamin A inhibited lipid peroxidation, elevated the activity of glutathine peroxidase and prevented a TCDD-induced decrease in GSH content in the liver. However, vitamin A did not inhibit the decrease in liver and body weights and provided little protection against TCDD-induced lethality. The activities of aryl hydrocarbon hydroxylase, glutathione-S-transferase (GST) and glutathione reductase (GR) increased after treatment with these two vitamins. Administration of vitamins E and A do not provide significant longterm protection against TCDD-induced lethality although they can prevent TCDD-induced microsomal lipid peroxidation as determined by the thiobarbituric acid assay method.     

电刺激对大鼠大脑、肝等组织脂质过氧化水平的影响

[目的 ]探讨电刺激应激对实验动物体内脂质过氧化水平以及抗氧化能力的影响。 [方法 ]采用 5 0Hz的强脉冲、电压为 10 0V交流电对实验大鼠连续 10d进行电刺激 ,观察受刺激后大鼠肝、大脑组织中抗氧化酶GSH Px、GST和抗氧化物质GSH以及反映脂质过氧化水平的脂质过氧化代谢产物MDA的含量。 [结果 ]受试大鼠肝和大脑组织中抗氧化物质GSH含量明显下降和MDA含量明显升高 ,抗氧化酶GSH Px、GST的活性明显下降 ,与对照组相比P <0 0 5和P <0 0 1。 [结论 ]电刺激应激能增强大鼠脑和肝组织脂质过氧化水平     

亚砷酸钠对大鼠肝线粒体和微粒体酶的影响

研究了亚砷酸钠在体内、体外对大鼠肝线粒体丙酮酸脱氢酶（ＰＤＨ）、琥珀酸脱氢酶（ＳＤＨ）和微粒体酶细胞色素Ｐ－４５０、ｂ５、ＮＡＤ（Ｐ）Ｈ－细胞色素Ｃ还原酶、谷胱甘肽硫转移酶（ＧＳＴ）的影响；并通过观测亚砷酸钠与亚硒酸钠的作用及其对肝谷胱甘肽过氧化物酶、谷胱甘肽含量和线粒体脂质过氧化的影响，探讨亚砷酸钠的作用机理。结果表明：连续７天腹腔注射２０ｍｇ／ｋｇ的亚砷酸钠，线粒体ＰＤＨ、ＳＤＨ被抑制，分别相当于对照组的５１％和５８％。而亚硒酸钠可有效拮抗砷对ＰＤＨ、ＳＤＨ的抑制作用。亚砷酸钠显著降低肝ＧＳＨ的含量，并增强线粒体膜脂质过氧化作用（Ｐ＜０．０５）。在体内试验中，亚砷酸钠对谷胱甘肽过氧化物酶和肝微粒体酶无明显影响。亚砷酸钠在体外实验中，浓度在１０－７～１０－３ｍｏｌ／Ｌ的范围内，抑制ＳＤＨ的活力，提高ＧＳＨ的含量，且呈剂量－效应关系。结果提示，亚砷酸钠对机体的作用与其对ＬＰＯ和体内巯基的影响有关     

Iron intake affects lipid peroxidation and glutathione peroxidase activity of distal colonic mucosa

The purpose of this study was to examine the effect of low, adequate, and high dietary iron (Fe) levels on lipid peroxidation, glutathione S-transferase (GST) and glutathione peroxidase (GSH-Px) activities, and glutathione (GSH) concentrations in colon and liver. Male Sprague Dawley rats were fed iron deficient (DFe; 14 mg Fe/kg diet; N=8), adequate iron (AFe; 39 mg Fe/kg diet, N=8), or high iron (HFe; 454 mg Fe/kg diet; N=8) diets for 3 weeks. Liver Fe concentrations were 26, 84, and 243 ug/g wet weight, respectively, for rats fed DFe, AFe, and HFe diets (p<0.0001). Lipid peroxidation was increased 70% in distal colonic mucosa of rats fed HFe diets compared to that of rats fed AFe and DFe diets (p<0.01), but lipid peroxidation was unaffected by diet in proximal colon or liver. While distal colonic mucosal GSH-Px activity was lower in DFe rats (0.062 U/mg protein), than in AFe rats (0.091 U/mg protein), and HFe rats (0.089 U/mg protein) (p<0.05), iron intake had no effect on GSH-Px activity in proximal colon or liver. The distal colon had higher GSH-Px activity than proximal colon (p<0.0001). GST activity in colon and liver, and hepatic GSH concentrations were not altered by dietary iron intakes. This study suggests that distal and proximal colonic mucosa may respond differently to changes in Fe status.     

扇贝提取物对肝损伤小鼠抗氧化功能的影响

目的　观察扇贝提取物 (SE)对肝损伤小鼠抗氧化功能的影响。方法　一次灌胃6% CCl4 油溶液 1 0 ml/kg bw,通过谷胱甘肽过氧化物酶 (GSH- Px)、超氧化物歧化酶 (SOD)、脂质过氧化物 (LPO)等指标观察给予 0 .5、1 .5、3.0 (g/kg)扇贝提取物的作用。结果　给予不同剂量扇贝提取物降低 LPO、提高 GSH- Px及 SOD的作用不同 ,以 1 .5g/kg bw效果最好。结论　扇贝提取物可能具有保护肝脏的作用     

Metallothionein induced by cadmium or zinc inhibits lipid peroxidation in rats exposed to dimethylnitrosamine

Dimethylnitrosamine (N-nitrosodimethyamine) is a potent inducer of microsomal lipid peroxidation in the liver and kidneys. The results of this study show that prior exposure of adult rats to cadmium or zinc antagonises the effect of dimethylnitrosamine on lipid peroxidation by inducing increased metallothionein synthesis. Increased concentration of reduced glutathione (GSH) in the liver and kidney of rats pre-treated with cadmium or zinc and exposed to dimethylnitrosamine suggests that metallothionein inhibits oxidative stress. The presented results have been corroborated by findings that exposure of adult rats to cadmium or zinc may activate genes for metallothionein and glutathione-S-transferase, the protective proteins against oxidative stress.     

烟叶硒蛋白在实验性小鼠肝损伤中的抗氧化作用

观察了烟叶硒蛋白（Ｓｅ－Ｒｕｂｉｓｃｏ）对四氯化碳肝损伤小鼠的保护作用。结果表明了一次灌胃６％四氯化碳油溶液１０ｍｌ／ｋｇｂｗ可使小鼠肝组织严重受损，谷胱甘肽过氧化物酶（ＧＳＨ－Ｐｘ）、超氧化物歧化酶（ＳＯＤ）活力急剧降低，脂质过氧化产物丙二醛（ＭＤＡ）显著上升。若提前补充烟叶硒蛋白或亚硒酸钠７ｄ，则可降低ＣＣｌ＿４对肝的损伤，并呈现出剂量效应关系，同时在抗脂质过氧化方面，硒蛋白明显优于亚硒酸钠和不含硒蛋白（Ｒｕｂｉｓｃｏ）组。     

Effects of progesterone on benzene toxicity in rats

Benzene is a frequently used industrial solvent. Its toxic manifestations could be modified by sex hormones, but mechanisms of their action are poorly understood. We have examined the influence of progesterone on lipid peroxidation (malondialdehyde), reduced glutathione (GSH), and cytochrome P450 2E1 (CYP2E1) in the liver and kidneys of female rats. Progesterone applied to benzene-treated rats inhibited the formation of reactive oxygen species (ROS), but in ovariectomised benzene-treated rats it significantly increased GSH in the liver. No improvement in CYP2E1 activity was observed in progesterone treated rats. Our results evidence that progesterone changes benzene toxicity (generation of ROS, oxidative stress). However, the probable antioxidative effect of progesterone needs to be confirmed by further studies.